Abnormalities of the cadherin-catenin complex in chemically-induced colo-rectal carcinogenesis

Tucker, Emma; Buda, Andrea; Janghra, Nari; Baker, Jenny A.; Coad, Joy; Moorghan, Morganden; Havler, Michael E.; Dettmar, Peter W.; Pignatelli, Massimo

doi:10.1079/pns2003217

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…This aberration has been strongly associated with specific tumors, such as lobular breast, diffuse-type gastric, and hepatocellular carcinomas, but it seems to be a rare event in CRC. In fact, a number of observations have described a decrease of E-cadherin expression in such neoplastic conditions [2,27,28], whereas other studies failed to demonstrate this finding [29,30,31]. In our study, only 4 tumors showed absence or marked reduction of E-cadherin expression in complete accordance with a recent article that observed this pattern in only 4 of 33 CRCs examined [32].…”

Section: Discussionsupporting

confidence: 93%

Down-regulation of μ-protocadherin expression is a common event in colorectal carcinogenesis

Losi¹,

Parenti²,

Ferrarini³

et al. 2011

Human Pathology

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Section: Discussionsupporting

confidence: 93%

Down-regulation of μ-protocadherin expression is a common event in colorectal carcinogenesis

Losi¹,

Parenti²,

Ferrarini³

et al. 2011

Human Pathology

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“…6A). Tet can inhibit DMH plus DSSinduced colon cancer, which is characteristic of β-catenin mutation and IGFBP-5 upregulation (49,52,53). Thus, the inhibitory effect of Tet on Wnt/β-catenin signaling transduction may not fully promote the degradation of β-catenin.…”

Section: Discussionmentioning

confidence: 99%

The role of IGFBP-5 in mediating the anti-proliferation effect of tetrandrine in human colon cancer cells

Zhou

et al. 2014

International Journal of Oncology

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Colon cancer is one of the most common malignancies, causes considerable morbidity and mortality. The current treatment for colon cancer is more modest than had been hoped. There is an urgent clinical need to explore new agents or adjuvants for colon cancer treatment. Natural products and their derivates act as one of the major source for anticancer agent. In the present study, we investigated the anti-proliferation and chemoprevention effects of tetrandrine (Tet) on colon cancer cells to uncover the possible molecular basis of this effect. We found that Tet can inhibit proliferation and induce apoptosis in LoVo cells. With dimethylhydrazine (DMH) and dextran sodium sulfate (DSS) induced colon cancer model, we found that Tet can prevent or inhibit DMH plus DSS induced aberrant crypt foci (ACF) and colon cancer formation, as well as suppress tumor growth in the xenograft colon cancer model. Tet can downregulate the expression of IGFBP-5 in LoVo cells. Exogenous expression of IGFBP-5 can attenuate the anti-cancer activity of Tet, while IGFBP-5 knockdown potentiates this effect of Tet on LoVo cells. Tet can inhibit Wnt/β-catenin signaling transduction, which can be partly reversed by exogenous expression of IGFBP-5, but is enhanced by IGFBP-5 knockdown. Our results demonstrated that the anticancer activity of Tet in colon cancer cells may be mediated partly by downregulating the expression of IGFBP-5, thus inactivating Wnt/β-catenin signaling transduction.

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“…β-Catenin is an essential component of junctional complexes, linking E-cadherin to the actin filaments [41]. Mouse studies of colorectal cancer have described increased cytoplasmic expression and nuclear localization of β-catenin in chemically induced tumours [42]. E-cadherin has also been shown to recruit β-catenin to the cell membrane and prevent its nuclear localization in SW480 colon carcinoma cells [43].…”

Section: Discussionmentioning

confidence: 99%

Induction of epithelial to mesenchymal transition in PMC42-LA human breast carcinoma cells by carcinoma-associated fibroblast secreted factors

et al. 2007

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BackgroundBreast carcinoma is accompanied by changes in the acellular and cellular components of the microenvironment, the latter typified by a switch from fibroblasts to myofibroblasts.MethodsWe utilised conditioned media cultures, Western blot analysis and immunocytochemistry to investigate the differential effects of normal mammary fibroblasts (NMFs) and mammary cancer-associated fibroblasts (CAFs) on the phenotype and behaviour of PMC42-LA breast cancer cells. NMFs were obtained from a mammary gland at reduction mammoplasty, and CAFs from a mammary carcinoma after resection.ResultsWe found greater expression of myofibroblastic markers in CAFs than in NMFs. Medium from both CAFs and NMFs induced novel expression of α-smooth muscle actin and cytokeratin-14 in PMC42-LA organoids. However, although conditioned media from NMFs resulted in distribution of vimentin-positive cells to the periphery of PMC42-LA organoids, this was not seen with CAF-conditioned medium. Upregulation of vimentin was accompanied by a mis-localization of E-cadherin, suggesting a loss of adhesive function. This was confirmed by visualizing the change in active β-catenin, localized to the cell junctions in control cells/cells in NMF-conditioned medium, to inactive β-catenin, localized to nuclei and cytoplasm in cells in CAF-conditioned medium.ConclusionWe found no significant difference between the influences of NMFs and CAFs on PMC42-LA cell proliferation, viability, or apoptosis; significantly, we demonstrated a role for CAFs, but not for NMFs, in increasing the migratory ability of PMC42-LA cells. By concentrating NMF-conditioned media, we demonstrated the presence of factor(s) that induce epithelial-mesenchymal transition in NMF-conditioned media that are present at higher levels in CAF-conditioned media. Our in vitro results are consistent with observations in vivo showing that alterations in stroma influence the phenotype and behaviour of surrounding cells and provide evidence for a role for CAFs in stimulating cancer progression via an epithelial-mesenchymal transition. These findings have implications for our understanding of the roles of signalling between epithelial and stromal cells in the development and progression of mammary carcinoma.

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Abnormalities of the cadherin-catenin complex in chemically-induced colo-rectal carcinogenesis

Cited by 12 publications

References 31 publications

Down-regulation of μ-protocadherin expression is a common event in colorectal carcinogenesis

Down-regulation of μ-protocadherin expression is a common event in colorectal carcinogenesis

The role of IGFBP-5 in mediating the anti-proliferation effect of tetrandrine in human colon cancer cells

Induction of epithelial to mesenchymal transition in PMC42-LA human breast carcinoma cells by carcinoma-associated fibroblast secreted factors

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